Endocrine Abstracts (2006) 11 P246

GH and GH antagonist B2036 effect on the immune system

M Maamra1, F Perna2, A Colao3, R Pivonello3, S Zappacosta5, RJM Ross1 & G Matarese4


1Division of Clinical Sciences (North), University of Sheffield, Sheffield, United Kingdom; 2Laboratorio di Immunologia A.O. Monaldi, Napoli, Italy; 3Department of Molecular and Clinical Endocrinology and Oncology, Federico II University of Naples, Napoli, Italy; 4Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, Napoli, Italy; 5Dipartimento de Biologia e Pathologia Cellulare e Molecolare, Federico II, University of Naples, Napoli, Italy.


Introduction: Growth Hormone (GH) receptors are expressed on, and GH is secreted by, human peripheral blood mononuclear cells (PBMCs). However, the role of GH in immunity has remained elusive and studies have given conflicting results. Experimental data strongly implicates a role for pituitary GH in the immune response of rodents. The data from knockout mice suggests that GH acts not as an obligate immunoregulator but as an anabolic and stress-modulating hormone. Despite the clear evidence for GH immunomodulatory actions in animal studies, the evidence from humans has been contradictory.

Aim: To clarify the role of GH in the human immunophenotype and human PBMCs proliferation.

Methods: Blood from GH deficient patients and patients with acromegaly (n=10), prior to treatment, was collected and PBMCs were immunophenotyped by FACS analysis (CD3, CD4, CD8, B, NK, NKT, CD4CD45RA, CD4CD45RO, CD4CD25, CD8CD28, gamma/delta, CD8CD45RA, CD8CD45RO). To analyse the effects on immune cell proliferation, PBMCs of normal individuals were isolated by Ficoll and the effects of GH and the specific GH antagonist B2036 were analysed after proliferation activation with anti-CD3 antibody (OKT3).

Results: Surface markers on T lymphocytes (CD3, CD4, CD8), B lymphocytes (CD19) and NK cells (CD16/56) were normal in all acromegalic and all but one GH deficient patient. This single GH deficient patient showed only elevated NK cells percentage. Neither GH at low (25 ng/ml) to high (500 ng/ml) concentrations, nor the GH antagonist B2036 nor the combination had any effect on the OKT3-induced proliferation of PBMCs whether with maximal or submaximal doses of OKT3.

Conclusions: GH status in patients did not seem to significantly influence the immune phenotype. Neither exogenous nor endogenous GH production by PBMCs influenced their proliferation. The results suggest that in contrast to rodents, GH in humans does not act as a strong immunoregulator.

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